final - ortho Flashcards

(34 cards)

1
Q

sport hx and physical

A

-Goal of preparticipation physical evaluation (PPE) -> promote health and safety
-Primary objectives: Screen for life-threatening or disabling conditions that may predispose to 2ndary injury/illness
-Secondary objectives: Establish a medical home, determine general health, assess fitness for specific sports, counseling on injury prevention and health related issues
-Ideal timing for exam is 6-8 weeks prior to training

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2
Q

sport preparticipation hx: cardiavascular hx

A

-Routine use of ECG and echo screening is debated
-Pertinent medical hx: Chest pain/discomfort with exercise, syncope/pre-syncope with exercise, excessive SOB or fatigue assoc with exercise, hx of heart murmur, hx of elevated BP
-Family hx: Premature death <50yo due to heart ds, disability from heart disease (< 50yo) in a close relative, knowledge of other specific cardiac conditions
-Physical: Auscultation of heart murmur in supine/standing position, palpation of radial, femoral pulses, physical stigmata of Marfan syndrome!, brachial BP in seated position
-Sudden cardiac arrest is leading cause of sudden death in young athletes
-No outcome-based studies that demonstrate effectiveness of PPE in preventing SCD in athletes
-MCC in U.S. is HCM and congenital coronary artery anomalies
-Any athletes with CVS sx require further eval before allowing sports
-Restrictions/disqualifications in consultation with cardiologist

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3
Q

sports preparticipation hx: hx of htn

A

-Any hx of HTN requires investigation for 2ndary causes and end-organ damage
-Athlete with HTN who exercises -> increases BP even more -> increases risk for complications
-Ask about stimulant use and family hx
-Athletes with pre-HTN are eligible to participate in sports (with counseling on lifestyle modifications)
-Athletes with stage I HTN in absence of end-organ damage may also participate in sports with appropriate subspecialist referral if symptomatic, has assoc heart ds/structural abnormality, or has persistent elevated BP on 2 additional occasions despite lifestyle modifications
-Athletes with stage II HTN or end-organ damage should not be cleared to participate in competitive sports until BP is evaluated, treated, and under control

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4
Q

sports preparticipation hx: CNS, chronic ds, surgical, mono, MSK, nutrition

A

-CNS: Hx of frequent exertional HA, seizure disorders, concussions/head injuries, recurrent stingers or burners, or cervical cord neuropraxia requires further eval, rehab, or informed decision-making prior to clearance
-Hx of Chronic Ds: Reactive airway disease, exercise-induced asthma, diabetes, renal ds, liver ds, chronic infections, or hematologic ds
-Surgical Hx: Full recovery with no long-term impact on athletic performance required prior to clearance
-Infectious Mono:
-Risk for splenic rupture is highest within first 3 weeks of illness and can occur in the absence of trauma
-Avoid physical activity during first 3-4 weeks after infection starts
-May return to sports once clinical symptoms are resolved/risk for splenic rupture assessed as minimal
-MSK- Limitations/Prior Injuries: Joints with limited ROM, muscle weakness
-Menstrual History: Presence of oligo- or amenorrhea (possible Female Athlete Triad/RED-S – caloric intake does not keep up with expenditure)
-Nutritional Issues- Assess RF for disordered eating or low energy availability -> May lead to persistent or recurrent injury, including bone stress injuries
-Vitamin D deficiency common in athletes
-Medication History: Rx, OTC, supplements
-Mental Health: Eating disorders, anxiety/depression screening

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5
Q

sports preparticipation physical

A

-routine vitals (including BP), cardiovascular exam, MSK exam, and other specific areas:
-Skin: Lesions (herpes, impetigo)
-Vision: Visual problems, retinal problems, eyes intact
-Abdomen: Hepatosplenomegaly
-GU: Testicular abnormalities, hernias
-Neurologic: Problems with coordination, gait, or mental processing
-Sexual Maturity: Tanner staging

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6
Q

sports clearance/recommendations

A

-Cleared for sports w/o restrictions
-Cleared for all sports w/o restrictions with recommendations for further eval or tx
-Not cleared pending further evaluation (for any sports, or for certain sports)
-Recommendations may be body system-specific

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7
Q

concussion

A

-Direct blow to body or head translates forces to brain -> transient alteration of neurologic function
-Usually not assoc with structural changes in brain detectable by imaging
-Sx evolve over first few hours
-Confusion, HA, visual disturbance, posttraumatic amnesia, balance alterations (does not have to involve LOC)
-suspected in any athlete with somatic, cognitive, or behavioral complaints
-resolve within 1-4wks
-Any suspicion -> immediately remove from play!
-Should not return same day of injury
-CT considered if deteriorating/AMS, prolonged LOC, repeated vomiting, severe HA, signs of skull fx, focal neurologic deficit, severe mechanism of injury
-CT Rarely indicated beyond first 24 hrs after injury

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8
Q

concussion tx

A

-Acute tx: Early physical and cognitive rest (1-2 days)
-Return to school with light noncontact physical activity -> early in recovery period
-Young athletes: Modified school attendance, decreased schoolwork, reduction in tech stimulation, proper nutrition/hydration, rest/sleep
-Before full return of sports: Sx resolved at rest and with exercise w/o aid of meds
-Return to play is 6-step process (each step 24 hrs):
-1. Asymptomatic at rest
-2. light aerobic exercise
-3. sport-specific exercise
-4. noncontact drills
-5. contact practice drills
-6. release to game play
-requiring medical clearance prior to return to sports (state dependent)
-Retirement from sports: Considerations include # of concussions, increasing frequency, occurrences with serially less force, prolonged/severe/permanent sx/signs

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9
Q

osgood schlatter disease (tibial tubercle apophysitis)

A

-Caused by recurrent traction on tibial tubercle apophysis
-occurs in jumping/running sports
-Fragmentation and microfractures of tibial tubercle
-occur during time of rapid growth
-pre-teen and adolescent years, -MC in boys 12-15 and girls 11-13 years
-Pain localized @ tibial tubercle -> aggravated by activities using eccentric quadriceps muscle movement
-Imaging: Fragmentation or irregular ossification of tibial tubercle
-Tx:
-Typically resolves spontaneously
-Pain control with NSAIDs
-PT and stretching the hamstrings/application of ice after workouts helpful

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10
Q

growing pains

A

-37% of school-age kids
-MC- 3-12yrs, M > F
-Deep, crampy pain in legs (not centered in joints)
-evening/nocturnal pain that awakens child from sleep
-exacerbated by activity
-dx based on hx and PE
-Tx:
-Reassurance and regular bedtime ritual of stretching and relaxation/massage, nighttime analgesic, resolution over time

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11
Q

torticollis

A

-Injury to SCM muscle during delivery or ds affecting cervical spine in infancy
-Chin rotates to side opposite of affected muscle causing head to tilt toward side of contracture
-May follow URI (swelling in upper cervical spine > rotary subluxation) or mild trauma
-Other causes: Tumors, syringomyelia, and RA
-Tx:
-Passive stretching effective in up to 97% of cases
-Surgical release of muscle origin and insertion

Head tilts toward the affected SCM (contracted side)

Chin rotates away from the affected side

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12
Q

scoloiosis**

A

-Lateral curvature of spine assoc w/ rotation of involved vertebrae and classified by anatomic location (thoracic or lumbar spine)
-4 categories: Idiopathic, congenital, neuromuscular, syndromic
-Idiopathic (80%): F > M, 10-12yo or sooner, genetic component/multifactorial etiology
-Congenital (5-7%): Vertebral abnormalities due to failure of formation or segmentation of affected vertebrae
-Typically, no back pain
-curvature of >= 30 degrees -> deformity of rib cage and asymmetry of waistline
-Lesser curves detected with Adams Forward Bend test
-Rotation of spine measured with scoliometer
-Assoc with marked rib hump and lateral curvature increases severity
-Imaging- radiographs of entire spine- standing (PA/lateral): Primary curve evident with compensatory curvature to balance body
-Tx:
-Depends on curve magnitude, skeletal maturity, and risk of progression
-dependent on Cobb angle – measured on standing PA x-ray
- < 20 degrees: No tx
- 20-40 degrees: Bracing in skeletally immature child
- > 40 degrees: Resistant to tx with bracing
-40-60 degrees: Surgical correctio -> Spinal instrumentation (rods, screws, hooks) and fusion (bone graft)
-Thoracic curvatures > 70 degrees: Poor pulmonary function

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13
Q

nursemaids elbow ** how to reduce it

A

-Subluxation of radial head as a result of being lifted or pulled by hand
-presents w/ elbow fully pronated and painful (point tenderness over radial head)
-Reduction: Palpable/audible click
-stabilize the radial head with one hand (thumb) -> Place elbow in full supination and slowly moving arm from full extension to full flexion
-Holding elbow at 90-degree angle of flexion, then slowly hyperpronating the wrist
-Following reduction, immediate relief of pain
-May immobilize in sling for comfort x 24hr (or longer, as needed)
-refractory- posterior splint and fu with ortho

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14
Q

growth plate fractures **

A

-Fx involving growth plate -> ~ 20% of all fx in skeletally immature pt
-MC- Distal radius, distal tibia, and distal fibula
-Growth plates are most susceptible to torsional and angular forces
-Described using Salter-Harris classification!!!!!!
-Type I: Transverse fracture through the physis; growth disturbance unusual
-Type II: Fracture through portion of physis and metaphysis; MC type (75%)
-Type III: Fracture through portion of physis and epiphysis; may result in complication because of intraarticular component/disruption of growing/hypertrophic zone of physis
-Type IV: Fracture through metaphysis, physis, and epiphysis; high risk of complication
-Type V: Crush injury to the physis with poor functional prognosis
-Tx:
-Types I and II: Closed reduction
-Types III and IV: Anatomic alignment for successful treatment
-Type V: Rare, often result in premature closing of the physis

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15
Q

torus (buckle) fracture

A

-very common
-kids bones bend
-wrist and ankle
-“buckling” of cortex due to compression of bone
-MC in distal radius or ulna (FOOSH injuries)
-Simple immobilization for 3wks typically sufficient (soft bandage/cast)

🧠 Mnemonic:
“Kids FOOSH → Cortex Squish”

Torus = Latin for “bulge” or “swelling”

FOOSH = Fall On OutStretched Hand → classic MOI

Cortex buckles, doesn’t break

🧱 Mental Image Hook
A kid’s bone = bendy plastic straw
Push the ends = it buckles at the middle, not breaks = torus fracture

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16
Q

supracondylar fx

A

-kid falling from monkey bar (fall from ht)
-Supracondylar region of humerus has thinner area of cortical bone -> more susceptible to injury/fx
-3-6yo
-MC elbow fx in kids
-Proximity to brachial artery in distal arm creates a potential danger
-Absence of distal pulse is a strong indicator of 2ndary arterial injury
-Swelling may be severe (usually assoc with significant amount of trauma)
-Dx- anterior and posterior fat pad (sale sign)
-Tx:
-Closed reduction with percutaneous pinning
-Complications: Volkmann ischemic contracture of the forearm due to vascular compromise and cubitus varus (“gunstock” deformity) 2ndary to poor reduction

17
Q

toddler’s fx

A

-trampoline, learning to walk
-Oblique fx of distal tibia w/o fibular fx
-typically, no significant trauma
-1-3yo, but can be as old as 6
-Present with limping and pain with wt-bearing versus minimal pain/swelling
-Initial x-ray may not show fx -> repeat in 7-10 days (with oblique view)
-Tx: Immobilization, usually heal within 3-4wks w/o disruption in growth

18
Q

osteogenesis imperfecta

A

-Genetic connective tissue ds characterized by multiple and recurrent fx
-1 in 12,000-15,000
-Several forms: Each assoc with mutation of different gene, varying levels of severity, and a range of characteristic features
-Severe fetal type: Multiple intrauterine or perinatal fx
-Moderately affected children: Numerous fx and exhibit dwarfism (acquired bone deformities and decreased growth velocity)
-Physical characteristics: Reduced cortical thickness in shafts of long bones, accessory skull bones, blue sclerae, thin skin, hyperextensibility of ligaments, otosclerosis with hearing loss, hypoplastic/deformed teeth
-Tx:
-Surgery: Correction of long bone deformities
-Intramedullary rods to decrease incidence of fractures and prevent deformity from fracture malunion

Individuals with osteogenesis imperfecta can’t BITE: Bones (recurrent fractures), I (“eye” = blue sclerae), Teeth (dental abnormalities), Ears (hearing loss).

Bone fractures from osteogenesis imperfecta are easily mistaken for signs of child maltreatment.

19
Q

developmental dysplasia of hip **

A

-abnormal relationship btwn proximal femur and acetabulum
-Dislocated hip: Femoral head is not in contact with acetabulum
-Dislocatable hip: Femoral head is within acetabulum, but can be dislocated with a provocative maneuver
-Subluxatable hip: Femoral head comes partially out of joint with provocative maneuver
-Acetabular dysplasia: Insufficient acetabular development (radiographic dx)
-4 major RF: 1st born child, female, breech, and family hx

20
Q

DDH: clinical manifestations **

A

-Clinical dx in newborns is dependent on demonstrating instability of joint by placing infant on back and obtaining complete relaxation
-Barlow sign: Adduction of hip (hip slips posteriorly) -> palpable “clunk” as head dislocates
-Ortolani sign: Hips flexed to 90 degrees, abducted from midline, attempt made to lift greater trochanter forward > feeling of “slipping” as head relocates
-Limited abduction (60 degrees) with hip at 90 degrees flexion is most sensitive sign for detecting a dysplastic hip
-Signs of instability less evident after first month of life
-Galeazzi sign: Knees at unequal heights when hips and knees flexed -> dislocated hip on side with lower knee
-Dx after walking begins:
-Painless limp/lurch to affected side
-Trendelenburg sign: Standing on affected leg > dip of pelvis evident on opposite side (weakness of gluteus medius muscle) = swaying gait
-B/L dislocation = waddling gait

21
Q

DDH: imaging and tx **

A

-Imaging:
-US- most useful in newborns
-Radiologic evaluation more valuable after first 6 weeks of life: Lateral displacement of femoral head
-Tx:
-Dysplasia is progressive with growth unless the instability is corrected – early diagnosis and treatment is therefore essential
-Pavlik harness: Maintains reduction by placing hip in a flexed and abducted position
-If hip cannot reduce easily on exam, Pavlik harness is CI
-Closed reduction with arthrogram, followed by hip spica cast
-Still unstable with closed reduction > open reduction

22
Q

avascular necrosis of proximal femur (Legg-Calve-Perthes) **

A

-Vascular supply to proximal femur is interrupted > necrosis of bone, followed by replacement (creeping substitution)
-Rapid growth of secondary ossification centers in epiphyses in relation to their blood supply subject them to avascular necrosis (also with trauma/infection)
-Highest incidence between 4 and 8 years of age
-Persistent pain with possible limp and/or limitation of motion
-Tx:
-Protection of joint by minimizing impact
-Nonoperative (casting) and surgical approaches to promote containment of the femoral head within the acetabulum and abduction of the hip
-Prognosis:
-Functional result following replacement of necrotic femoral head depends on the amount of deformity that has developed
-Better outcomes for < 6 years of age
-Poorer prognosis for older aged children, more completed involvement of epiphyseal center, metaphyseal defects, more complete involvement of femoral head

23
Q

avascular necrosis of proximal femur (legg-calve-perthes)- imaging **

A

-IMAGING STAGES ARE NOT ON TEST
-Early findings: Effusion of the joint associated with slight widening of the joint space and periarticular swelling
-Few weeks: Decreased bone density in and around the joint
-Necrotic ossification center appears denser than surrounding viable structures and femoral head is collapsed or narrowed
-Fragmentation of epiphysis as replacement of necrotic ossification center occurs
-Widening of femoral head with flattening/coxa plana
-If infarction extends across growth plate > radiolucent lesion within metaphysis
-If growth center of the femoral head has been damaged and normal growth arrested > shortening of femoral neck
-Eventually, complete replacement of epiphysis
-Final shape of head depends on the extent of the necrosis and collapse of weakened bone

Early: widened joint space + soft tissue swelling

Mid: dense, fragmented femoral head

Late: flattened, widened head (coxa plana)

Severe: growth plate damage → short femoral neck

24
Q

slipped capital femoral epiphysis (SCFE): dx and tx **

A

-Physical: Limitation of internal rotation of the hip

-Imaging: AP/lateral pelvis radiograph
-Steel sign, widening of physis on affected side, epiphysis below Klein line
-kline should go through epiphysis

-Tx:
-NWB on crutches and immediate referral to an orthopedic surgeon
-ORIF is standard of care due to high risk of AVN of femoral head associated with closed reduction

-Prognosis is guarded:
-Most patients continue to be overweight and overstress hip joints
-High rate of premature degenerative arthritis (even without AVN)
-30% of pts have B/L involvement which may occur as late as 1 or 2 years after primary episode

rf: obese, AA; needs ORIF
\Obese adolescent with hip/knee pain + limited internal rotation

Get AP + frog-leg lateral pelvis X-rays

Look for Klein’s line missing the epiphysis

Tx = urgent ortho + in situ pinning

25
femoral anteversion/tibial torsion (intoeing)
-Intoeing is usually due to either femoral anteversion or tibial torsion -Femoral anteversion: Internal rotation of the knees, compared to hips -Tibial torsion: Rotation of leg between knee and ankle -No gait/ambulatory issues, but may cause tripping during running activities -Typically, more noticeable later in day due to weakness of the hip external rotator musculature (used to compensate for intoeing throughout the day) -Both largely self-limiting -Tibial torsion remodeling up to 8-10 years in females, 10-12 years in males -Femoral anteversion remodeling another 2-4 years past tibial torsion remodeling -Tx: -Education/reassurance -No work-up unless persistence past 8-10 years of age and/or causing functional ambulatory issues -Physical therapy -Surgical treatment for true bone rotational deformity (if symptomatic)
26
genu varum/valgum
-Genu varum (bowleg) is normal from infancy through 3 years of age > then alignment changes to genu valgum (knock-knee) until ~ 8 years of age > adult alignment (5-9 degrees of anatomic valgus) -Orthopedic referral if: -Bowing persists past 2 years of age, increases rather than decreases, occurs only in 1 leg -Knock-kneed in association with short stature -Pathological genu varum is usually secondary to tibial rotation (Blount disease) -Pathological genu valgum is usually caused by skeletal dysplasia or rickets -Tx: -Individuals with genu varum may be at future risk for OA – bracing may be appropriate -Osteotomy for severe problems
27
talipes equinovarus (clubfoot)
-1-2/1,000 live births -3 features required for dx: -Plantar flexion of foot at the ankle joint (equinus) -Inversion deformity of the heel (varus) -Medial deviation of the forefoot (adductus) -3 categories: Idiopathic (hereditary component), neurogenic, and those associated with syndromes -Treatment -Manipulation of foot to stretch contracted tissues on medial/posterior aspects followed by casting (Ponseti technique) -Serial castings performed on a weekly basis x 6-8 weeks -If remaining equinus following casting > surgery (Achilles tenotomy) -After full correction: Night brace for long-term maintenance
28
metatarus adductus
-Congenital foot deformity, characterized by inward deviation of the forefoot -MC foot abnormality (1-2/1,000 live births) -Rigid versus flexible deformities -Most flexible deformities from intrauterine positioning and usually resolve spontaneously -TX: -Flexible: No treatment -Rigid: Serial casting with cast changes every 1-2 weeks
29
transient synovitis ***
-MC cause of limping and hip pain in children in the U.S. (3-10 years) -Self-limiting, acute inflammatory reaction often following an upper respiratory or GI infection -Hip joint experiences limited ROM, particularly internal rotation -Radiographic findings are nonspecific; some swelling apparent in soft tissues around joint -Must differentiate from septic arthritis! -No elevation in ESR, WBC count, or fever > 38.3C; clear aspirate from joint (if performed) -More definitively distinguished from septic arthritis with a dynamic contrast enhanced MRI -Tx: -Rest and NSAIDs -Radiographic follow-up important: May be precursor to AVN of femoral head (6 weeks or earlier if limp persists)
30
pyogenic (septic) arthritis **
-Source varies according to age -Infantile: Adjacent osteomyelitis -Older kid: Isolated infection w/o bony involvement -Teens: Underlying systemic ds or organism that has affinity for joints (Neisseria gonorrhoeae) -MC organism varies by age -< 4mo: GBS, S. aureus -4mo–4yrs: H. influenza B (if unimmunized), S. aureus -Older kids/adolescents: S. pyogenes, S. aureus, S. pneumoniae, N. meningitidis, N. gonorrhoeae -Kingella kingae is a gram-neg bacterium increasingly recognized as cause in < 5yo -Initial effusion rapidly becomes purulent -> may affect adjacent bone -Infants: Decreased abduction of hip, irritable, or feeding poorly -Older kids: Fever, malaise, vomiting, restriction of motion, joint swelling, warmth, erythema, and/or tenderness -Imaging: -Plain radiograph: -Dislocation of joint (within days) -Destruction of joint space, resorption of epiphyseal cartilage, erosion of adjacent bone of metaphysis (later) -Bone scan: Increased flow and uptake about joint -MRI/US: Joint effusion detection
31
pyogenic (septic) arthritis tx. **
-Aspiration of joint for dx -Need for aspiration evaluated with Kocher criteria -NWB, ESR > 40 mm/h, temp > 38.5C, WBC > 12K cells/mm^3, CRP > 2.0 mg/dL -Surgical drainage with WBCs > 30-50K cells/mm^3 followed by appropriate antibiotic therapy -Empiric: Nafcillin, oxacillin + third generation cephalosporin -Antistaphylococcal agent alone usually adequate > 5 years (unless gonococcal/meningococcal infection suspected) -Prognosis: Excellent prognosis if joint drained before damage to articular cartilage (> 24 hours) and/or growth plates
32
juvenile idiopathic arthritis (test) **
-Oligoarticular (MC form, 40-60%): 4 or fewer joints, medium to large joints, asymmetrical (children may develop leg-length discrepancy) -20% develop !!asymptomatic uveitis (may cause blindness) -Polyarticular (20-35%): 5 or more joints, large and small joints, symmetrical -Low grade fever, fatigue, rheumatoid nodules, and anemia may be present -Further divided into !RF-positive versus RF-negative: Positive is more chronic, destructive arthritis -Systemic (10-15%): Any number of joints, large and small joints -High fever (39-40C), typically 1-2 times per day -~80-90% of patients have evanescent, salmon-pink macular rash! that is most prominent on pressure areas, especially when fever is present -Other systemic features: Hepatosplenomegaly, lymphadenopathy, leukocytosis, and serositis -Enthesitis-associated (5-10%): MC in males older than 10 years of age, typically, associated with lower extremity, large joints, hallmark is inflammation of tendinous insertions (enthesitis) -Low back pain and sacroiliitis also common -Psoriatic -May have typical psoriasis or more subtle changes, like nail pitting -May have dactylitis (“sausage digit!”) – painful swelling of entire finger or toe -Undifferentiated (10% of patients): Chronic arthritis without meeting criteria for any of the other subgroups or meet more than one criterion that classify them into multiple subgroups
33
juvenile idiopathic arthritis dx **
-Labs: -No diagnostic test for JIA -Markers: -ANA associated with increased risk of uveitis in those with oligoarticular disease and those with late-onset, RF-positive form of disease -RF is positive in ~5% of patients (usually when polyarticular form occurs after 8 years of age) -Anti-CCP has high specificity for RA and may be elevated prior to RF -Systemic JIA: Significantly elevated markers of inflammation (ESR, CRP, WBCs, platelets) -HLAB27 antigen associated with increased risk of developing enthesitis form -Joint aspiration performed to rule out infection -JIA: 5K-60K WBCs/uL, glucose usually normal or slightly low -Imaging -Early disease: -Plain films: Soft tissue swelling, periarticular osteoporosis -MRI: Early joint damage; if with gadolinium, can confirm presence of synovitis -US: Synovitis, tenosynovitis, and bony erosions -Later disease: Plain films: Joint space narrowing, erosive changes of bone related to chronic inflammation
34
juvenile idiopathic arthritis tx **
-Objectives are to restore function, relieve pain, maintain joint motion, and prevent damage to cartilage and bone -!!NSAIDs: Naproxen, ibuprofen, meloxicam -Symptomatic improvement after 1 month or up to 8-12 weeks -Disease-Modifying Agents: Methotrexate, leflunomide, JAK inhibitors -Weekly methotrexate: Response within 3-4 weeks, CBC and LFTs every 2-3 months -Biologic Agents (inhibit TNF): Etanercept, infliximab, adalimumab, rituximab, abatacept -Corticosteroids: -Local injections with triamcinolone acetonide -PO/parenteral for severe involvement/systemic disease -Uveitis: Corticosteroid drops and dilating agents to prevent scarring between iris and lens -Systemic medications for failure of topical treatments -Rehabilitation: -PT/OT to focus on ROM, stretching, and strengthening -Leg-length discrepancy: Shoe lift on shorter side -Prognosis: -Variable, based on subtype -Persistent oligoarticular have highest rate of clinical remission -RF-positive disease least likely to achieve remission and highest risk for chronic, erosive arthritis -Systemic disease worse in those with persistent symptoms past 6 months, thrombocytosis, and more extensive arthritis